Elementary events in excitation-contraction coupling of the mammalian myocardium

1977 ◽  
pp. 48-54
Author(s):  
H. Antoni
Keyword(s):  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Mammalian Myocardium

Frog ventricle: participation of SR in excitation-contraction coupling

1989 ◽  
Vol 256 (5) ◽  
pp. H1432-H1439
Author(s):  
M. E. Anderson ◽  
I. J. Fox ◽  
C. R. Swayze ◽  
S. K. Donaldson
Keyword(s):  
Steady State ◽  
Sarcoplasmic Reticulum ◽  
Inhibitory Effects ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Resting Tension ◽  
Mammalian Myocardium ◽  
Frog Myocardium ◽  
Frog Ventricle ◽  
Important Site

Activation of the first beat (B1) following a 60-s pause is diminished in isometrically contracting frog ventricular strips, in contrast to the augmentation documented for sarcoplasmic reticulum (SR)-dependent mammalian myocardium. However, treatment of frog ventricular strips with ouabain, an indirect inhibitor of the sarcolemmal Na+-Ca2+ exchanger, selectively enhanced postpause beats suggesting that in the absence of ouabain significant extrusion of cellular Ca2+ occurred during the pause. Because resting tension did not increase during the pause in ouabain-treated strips, the nonextruded Ca2+ must have been sequestered into a compartment such as SR. Steady-state beats were not affected by ouabain; its actions appeared to be separate from its known positive inotropism. Caffeine, a direct SR stimulus, initially enhanced B1 and subsequently decreased activation of all beats, which was consistent with initial augmentation of SR Ca2+ release and subsequent depletion of SR Ca2+ stores. Ouabain both potentiated the stimulatory effects and blocked the inhibitory effects of caffeine, suggesting that ouabain increased Ca2+ stores in the same intracellular Ca2+ pool as that acted on by caffeine, the SR. Ryanodine, an inhibitor of SR in mammalian myocardium, did not affect activation of frog myocardium. SR may be an important site for activator Ca2+ cycling in frog myocardium under control conditions as well as after long diastolic intervals in the presence of ouabain.

scholarly journals Remodeling of t-system and proteins underlying excitation-contraction coupling in aging versus failing human heart

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yankun Lyu ◽  
Vipin K. Verma ◽  
Younjee Lee ◽  
Iosif Taleb ◽  
Rachit Badolia ◽  
...  
Keyword(s):  
Heart Function ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Excitation Contraction Coupling ◽  
Transverse Tubular System ◽  
Contraction Coupling ◽  
Senescent Phenotype ◽  
Cellular Microstructure ◽  
T System

AbstractIt is well established that the aging heart progressively remodels towards a senescent phenotype, but alterations of cellular microstructure and their differences to chronic heart failure (HF) associated remodeling remain ill-defined. Here, we show that the transverse tubular system (t-system) and proteins underlying excitation-contraction coupling in cardiomyocytes are characteristically remodeled with age. We shed light on mechanisms of this remodeling and identified similarities and differences to chronic HF. Using left ventricular myocardium from donors and HF patients with ages between 19 and 75 years, we established a library of 3D reconstructions of the t-system as well as ryanodine receptor (RyR) and junctophilin 2 (JPH2) clusters. Aging was characterized by t-system alterations and sarcolemmal dissociation of RyR clusters. This remodeling was less pronounced than in HF and accompanied by major alterations of JPH2 arrangement. Our study indicates that targeting sarcolemmal association of JPH2 might ameliorate age-associated deficiencies of heart function.

scholarly journals 112 THE AGE DEPENDENCY OF MYOCARDIAL EXCITATION CONTRACTION COUPLING

1985 ◽  
Vol 19 (4) ◽  
pp. 129A-129A
Author(s):  
Thomas S Klitzner ◽  
William F Friedman
Keyword(s):  
Age Dependency ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling
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